18 results on '"L. Schewior"'
Search Results
2. Massive haemolysis after intramuscular diclofenac in a patient who apparently tolerated oral medication
- Author
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Edeltraut Garbe, Abdulgabar Salama, L. Schewior, Holger Kiesewetter, and Norbert Ahrens
- Subjects
Anemia, Hemolytic ,medicine.medical_specialty ,Diclofenac ,Nausea ,610 Medizin ,Administration, Oral ,Injections, Intramuscular ,Gastroenterology ,Antibodies ,Diagnosis, Differential ,Oral administration ,Internal medicine ,medicine ,Humans ,Renal Insufficiency ,Aged ,business.industry ,diclofenac, drug-dependent antibodies, drug-induced haemolysis, immunehaemolytic anaemia ,Autoantibody ,Hematology ,General Medicine ,Jaundice ,Haemolysis ,Surgery ,stomatognathic diseases ,Prednisolone ,Female ,Anemia, Hemolytic, Autoimmune ,medicine.symptom ,Intramuscular injection ,business ,medicine.drug - Abstract
Background and Objectives Administration of diclofenac may lead to immune haemolytic anaemia (IHA) owing to the presence of drug-dependent antibodies and/or autoantibodies. A relationship with oral or intramuscular drug administration is unknown. Here, we describe a patient who apparently tolerated oral diclofenac but developed severe IHA following intramuscular injection of the drug. Patients and Methods A 66-year-old-female was admitted to hospital because of jaundice and nausea, which were initially presumed to be manifestations of a postcholecystectomy syndrome. The patient soon developed haemolysis and renal failure. Although the symptoms and signs were suggestive of autoimmune haemolytic anaemia (AIHA), the patient had diclofenac-induced IHA. Results Serological testing, including detection of drug-dependent antibodies, was performed using standard techniques. The patient's serum was found to contain a highly reactive diclofenac-dependent red cell antibody of the immune complex type (titre 256 000). She recovered after 7 weeks of treatment with prednisolone, blood transfusions, haemodialysis and plasma exchange. Conclusions Diclofenac-induced IHA should always be considered when a patient on diclofenac develops haemolysis.
- Published
- 2004
3. Acute renal failure after liver transplantation: incidence, etiology, therapy, and outcome
- Author
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Andreas Kahl, Stefan G. Tullius, S Kohler, Ulrich Frei, Ruth Neuhaus, Jan M. Langrehr, Peter Neuhaus, G. Junge, and L. Schewior
- Subjects
Male ,medicine.medical_specialty ,medicine.medical_treatment ,Renal function ,Liver transplantation ,Gastroenterology ,Blood Urea Nitrogen ,chemistry.chemical_compound ,Postoperative Complications ,Hepatorenal syndrome ,Internal medicine ,medicine ,Humans ,Retrospective Studies ,Transplantation ,Creatinine ,business.industry ,Incidence ,Graft Survival ,Hepatitis C ,Acute Kidney Injury ,Middle Aged ,medicine.disease ,Prognosis ,Survival Analysis ,Surgery ,Liver Transplantation ,surgical procedures, operative ,Treatment Outcome ,chemistry ,Kidney Failure, Chronic ,Female ,Hemodialysis ,business ,Kidney disease - Abstract
Acute renal failure (ARF) was a frequent complication after orthotopic liver transplantation (OLT) when ARF was defined by a calculated glomerular filtration rate decrease of >50% or by a doubled serum creatinine above 2.5 mg/dL within the first week after OLT. We analyzed 1352 liver transplant recipients in retrospective fashion with regard to the incidence, etiology, therapy, and outcome of ARF; 162 patients developed ARF within the first week after OLT (12%), among whom 157 patients (97%) were recompensated by postoperative day 28. Altogether 52 patients (32%) received an average of 6 hemodialysis treatments, excluding the 5 patients (3%) who developed end-stage renal failure. Risk factors for this complication included hepatorenal syndrome type II, a glomerular filtration rate of
- Published
- 2006
4. Small volume hypertonic hydroxyethyl starch reduces acute microvascular dysfunction after closed soft-tissue trauma
- Author
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Michael D. Menger, L. Schewior, Michael Raschke, Thomas Mittlmeier, K.-D. Schaser, and Brigitte Vollmar
- Subjects
Male ,Pathology ,medicine.medical_specialty ,Soft Tissue Injuries ,medicine.medical_treatment ,Hypertonic Solutions ,Plasma Substitutes ,Hydroxyethyl starch ,Microcirculation ,Extensor digitorum longus muscle ,Hydroxyethyl Starch Derivatives ,Rats, Sprague-Dawley ,Edema ,medicine ,Laser-Doppler Flowmetry ,Animals ,Orthopedics and Sports Medicine ,Vascular Diseases ,Saline ,business.industry ,Laser Doppler velocimetry ,Rats ,Anesthesia ,Acute Disease ,Tonicity ,Surgery ,medicine.symptom ,business ,Intravital microscopy ,medicine.drug - Abstract
A major pathway of closed soft-tissue injury is failure of microvascular perfusion combined with a persistently enhanced inflammatory response. We therefore tested the hypothesis that hypertonic hydroxyethyl starch (HS/HES) effectively restores microcirculation and reduces leukocyte adherence after closed soft-tissue injury. We induced closed soft-tissue injury in the hindlimbs of 14 male isoflurane-anaesthetised rats. Seven traumatised animals received 7.5% sodium chloride-6% HS/HES and seven isovolaemic 0.9% saline (NS). Six non-injured animals did not receive any additional fluid and acted as a control group. The microcirculation of the extensor digitorum longus muscle (EDL) was quantitatively analysed two hours after trauma using intravital microscopy and laser Doppler flowmetry, i.e. erythrocyte flux. Oedema was assessed by the wet-to-dry-weight ratio of the EDL. In NS-treated animals closed soft-tissue injury resulted in massive reduction of functional capillary density (FCD) and a marked increase in microvascular permeability and leukocyte-endothelial cell interaction as compared with the control group. By contrast, HS/HES was effective in restoring the FCD to 94% of values found in the control group. In addition, leukocyte rolling decreased almost to control levels and leukocyte adherence was found to be reduced by ~50%. Erythrocyte flux in NS-treated animals decreased to 90 ± 8% (mean sem), whereas values in the HS/HES group significantly increased to 137 ± 3% compared with the baseline flux. Oedema in the HS/HES group (1.06 ± 0.02) was significantly decreased compared with the NS-group (1.12 ± 0.01). HS/HES effectively restores nutritive perfusion, decreases leukocyte adherence, improves endothelial integrity and attenuates oedema, thereby restricting tissue damage evolving secondary to closed soft-tissue injury. It appears to be an effective intervention, supporting nutritional blood flow by reducing trauma-induced microvascular dysfunction.
- Published
- 2003
5. Experimentelle Unfallchirurgie III Preisträgersitzung
- Author
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Harald Hertz, Thomas L. Smith, G. Peters, Burkhard W. Wippermann, Gerhard Schmidmaier, A. Weiler, M. Fehr, Brigitte Vollmar, A. Ignatius, V. Vecsei, Thomas Mittlmeier, H. Tscherne, W. Seidl, M. Grotz, R. Wenz, M. Schnabel, M. Raschke, Britt Wildemann, G. Schlag, A. Kröpfl, L. Schewior, S. Marlovits, W. W. Curl, M. v. Griensven, N. P. Haas, H. Redl, W. Linhart, U. Berger, K. J. McLeod, M. D. Menger, P. Patka, L. Gotzen, L. Claes, H. C. Pape, G. Eckhoff, J. Schlegel, J. M. Rueger, F. N. Unterhauser, Klaus-D. Schaser, H. J. Bail, J. Mäurer, D. Kaspar, F. Zailskas, Wolfgang A. Menth-Chiari, D. W. Sommerfeldt, N. P. Südkamp, and T. Blokhuis
- Published
- 2000
6. In vivo analysis of microcirculation following closed soft-tissue injury
- Author
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K D, Schaser, B, Vollmar, M D, Menger, L, Schewior, S N, Kroppenstedt, M, Raschke, A S, Lübbe, N P, Haas, and T, Mittlmeier
- Subjects
Male ,Soft Tissue Injuries ,Microcirculation ,Blood Pressure ,Cell Communication ,Rats ,Capillary Permeability ,Rats, Sprague-Dawley ,Disease Models, Animal ,Heart Rate ,Cell Adhesion ,Leukocytes ,Pressure ,Animals ,Edema ,Endothelium, Vascular ,Muscle, Skeletal - Abstract
Major loss of tissue is an almost invariable consequence of severe closed soft-tissue injury. Clinically, the extent of soft-tissue trauma determines the outcome of complex injuries and significantly influences bone healing. With use of a new animal model, this study quantitatively analyzed microcirculation, i.e., nutritive perfusion and leukocyte-endothelial cell interaction, in skeletal muscle after standardized closed soft-tissue injury. By means of a computer-assisted controlled-impact technique, a severe standardized closed soft-tissue injury was induced in the left hindlimb of 28 rats. The rats were assigned to four experimental groups (n = 7 per group) that differed by time of analysis (1.5, 24, 72, and 120 hours after injury); rats that were not injured served as controls (n = 7). Intramuscular pressure was measured, and microcirculation in the rat extensor digitorum longus muscle was analyzed by in vivo fluorescence microscopy, which allowed assessment of microvascular diameters, functional capillary density, number of rolling and adherent leukocytes in venules, and microvascular permeability. Edema weight gain was quantified by the ratio of wet to dry weight of the extensor digitorum longus muscle. Microvascular perfusion of the skeletal muscle was characterized by a significant reduction in functional capillary density, which was paralleled by an increase in capillary diameter throughout the 120 hours of observation when compared with the controls. Trauma-induced inflammatory response was reflected by a markedly increased rolling and adherence of leukocytes, primarily restricted to the endothelium of postcapillary venules; this was accompanied by increased microvascular permeability, indicative of a substantial loss of endothelial integrity. The microcirculation surrounding the core of the damaged tissue area resembled that of ischemia-reperfusion injury in skeletal muscle, i.e., heterogeneous capillary perfusion, pronounced microvascular leakage, and adherence of leukocytes. Enhanced vascular leakage and leukocyte adherence (24-72 hours after injury) coincided with the maximum intramuscular pressure (which was not indicative of compartment syndrome) and edema formation. These results demonstrate that initial changes, leading to ultimate tissue death, after closed soft-tissue injury are caused on the microcirculatory level. This standardized model provides further insight into microvascular pathophysiology and cellular interactions following closed soft-tissue injury. Thus, it is an adequate tool for testing novel therapeutic interventions.
- Published
- 1999
7. Experimentelle Traumatologie
- Author
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T. Schmickal, B. Biglari, A. Wentzensen, D. Hadler, H. R. Kortmann, M. Schlüter, S. Fuchs, M. Maghsudi, B. Füchtmeier, R. Hente, M. Nerlich, K. Eckert-Hübner, L. Claes, G. N. Duda, N. Haas, A. Pommer, D. Richter, M. P. Hahn, G. Muhr, M. Amlang, T. Illert, K. Nestler, G. Weiss, H. Zwipp, C. Lill, A. Flügel, G. v. Salis, E. Schneider, A. Rübbert, H. Thermann, R. Hoffmann, A. Weiler, S. Scheffler, N. Südkamp, V. Mengel, C. Hoffmann, A. Janousek, J. Pfiel, S. Wolf, H. Hertz, G. Schlag, A. Junge, M. El-Sheik, I. Celik, L. Gotzen, C. Voigt, C. Müller-Mai, U. Gross, K. Kandilakis, R. Rahmanzadeh, P. Zouboulis, P. Megas, A. Karabasi, E. Lambiris, G. Voggenreiter, St. Assenmacher, L. C. Olivier, F. Adam, D. Kohn, J.-F. Lataste, P. E. Zouboulis, B. Clasbrummel, M. Walz, G. Schütte, D. Rosenbaum, H. Witte, U. Schümann, D. Wolter, L. L. Latta, A. Ekkernkamp, P. A. W. Ostermann, G. Suger, A. Laule, L. Kinzl, S. Tepic, B. Rahn, S. M. Perren, M. Raschke, A. Stemberger, H. Bail, K. Schaser, D. J. Schaefer, G.B Stark, G. Herr, A. Menke, G. Hobom, R. Schnettler, S. Verelst, R. Wirbel, W. Mutschler, M. Keel, U. Ungethüm, T. Hartung, W. Ertel, W. A. Menth-Chiari, W. W. Curl, V. Vecsei, T. L. Smith, C. Klemt, C. Andree, H. P. Friedl, A. Baltzer, C. Lattermann, P. Robbins, C. Evans, H. Schmal, B. J. Czermak, N. M. Bless, M. Jonas, J. Raunset, J. Enczmann, P. Wernet, P. Angele, R. Kujat, H. Faltermeier, H. D. Moeller, C. Englert, D. Schmitz, S. Flohé, U. Obertacke, F. U. Schade, I. Fichtel, M. Schnabel, J. Schlegel, L. Schewior, B. Vollmar, G. Duda, J. Hoffmann, T. Mittlmeier, M. Grasslober, S. Marlovits, F. Kutscha-Lissberg, V. Vécsei, M. van Griensven, A. Seekamp, K. Rother, G. Regel, S. Kroppenstedt, M. Menger, K. Wolf, J. Hamar, A. Pethes, S. Moravec, T. Farkas, L. Schweiberer, R. H. Richter, R. Schwille, C. O. R. Grüneis, F. F. Hennig, M. Raum, D. Rixen, B. Holzgraefe, H.-J. Goller, E. Neugebauer, T. Tiling, C. Göpfert, N. M. Meenen, J.-P. Petersen, J. Seitz, P. Adamietz, D. W. Sommerfeldt, W. Linhart, J. Windolf, J. M. Rueger, U. Horas, D. Pelinkovic, M. Börner, M. Clathworthy, F. H. Fu, C. H. Evans, A. Häring, M. Köller, M. Wick, M. Reuter, S. Bahrami, M. Ackermann, H. Redl, J. Löhnert, S. Kolbeck, I. Ahnfeld-Roenne, N. P. Haas, A. Gomoll, G. Metak, M. Scherer, R. Ascherl, E. Mayr, A. Rüter, U. Bosch, J. Zeichen, P. Lobenhoffer, E. Schratt, T. Kalteis, J. Grifka, W. Plitz, M. Kramer, P. Katzmaier, E. Hartwig, R. Peine, A. Hennerbichler, M. Kirschner, G. O. Hofmann, O. Gaber, M. Brauckmann, M. Krieger, J. Pfeil, F. E. Isemer, B. Wippermann, J. Wefer, A. Kniesch, H. Tscherne, H.-E. Schratt, M. Grotz, A. Mayer, M. Hansen, G. Aue, D. Peetz, W. Prellwitz, P. M. Rommens, H. Lill, T. Engel, P. Verheyden, C. Josten, G. Kelsch, E. Savvidis, and K. Parsch
- Published
- 1999
8. Withdrawal of Steroids: A Randomized Prospective Study of Prednisone and Tacrolimus Versus Mycophenolate Mofetil and Tacrolimus in Liver Transplant Recipients With Autoimmune Hepatitis
- Author
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Olaf Guckelberger, L. Schewior, J Klupp, Stefan G. Tullius, Peter Neuhaus, Ruth Neuhaus, Jan M. Langrehr, and G. Junge
- Subjects
Adult ,Male ,medicine.medical_specialty ,Time Factors ,Anti-Inflammatory Agents ,Autoimmune hepatitis ,Gastroenterology ,Drug Administration Schedule ,Tacrolimus ,Mycophenolic acid ,Maintenance therapy ,Bone Density ,Prednisone ,Internal medicine ,medicine ,Humans ,Antibacterial agent ,Glycated Hemoglobin ,Hepatitis ,Transplantation ,business.industry ,Mycophenolic Acid ,medicine.disease ,Liver Transplantation ,Hepatitis, Autoimmune ,surgical procedures, operative ,Immunology ,Drug Therapy, Combination ,Female ,Surgery ,business ,Immunosuppressive Agents ,Follow-Up Studies ,medicine.drug - Abstract
The aim of this study was to evaluate the success of steroid (PRED) withdrawal due to replacement by mycophenolate mofetil (MMF) in orthotopic liver transplant (OLT) recipients with autoimmune hepatitis (AIH). Thirty patients with AIH > 12 months after OLT randomized to receive either PRED and tacrolimus (TAC) or MMF and TAC were followed for 24 months. Withdrawal of steroids showed no difference regarding graft and patient survival. Also we demonstrated significantly lower glucose levels with lower HbA1c and a reduced need for insulin as well as a significantly lower serum cholesterol in the MMF group. Patients without steroids showed a lower incidence of osteopenia. Maintenance therapy in OLT patients with AIH may be performed safely using MMF instead of prednisone.
- Published
- 2005
9. The Influence of Late Acute Rejection Episodes on Long-Term Graft Outcome After Liver Transplantation
- Author
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C. Radke, Peter Neuhaus, Ruth Neuhaus, L. Schewior, G. Junge, Stefan G. Tullius, Johann Pratschke, and V. Klitzing
- Subjects
Graft Rejection ,medicine.medical_specialty ,Time Factors ,Graft failure ,medicine.medical_treatment ,Liver transplantation ,Organ transplantation ,Transaminase ,Liver Function Tests ,Humans ,Medicine ,Risk factor ,Organ system ,Retrospective Studies ,Transplantation ,business.industry ,Incidence (epidemiology) ,Survival Analysis ,Liver Transplantation ,Surgery ,Treatment Outcome ,surgical procedures, operative ,Acute Disease ,business ,Follow-Up Studies - Abstract
Acute cellular rejection represents the most important single risk factor for the occurrence of chronic rejection after organ transplantation. We correlated late acute rejections with the occurrence of chronic graft failure after liver transplantation. We followed 1426 liver transplants for late acute rejection episodes defined as occurring >3 months after OLT. The overall incidence of chronic rejection in our patient population was 3.7%. In summary, we observed a predictive increase of transaminase levels prior to routine biopsies among patients with histologic evidence of late acute rejections. In contrast to other organ systems, late acute rejection episodes were not associated with the occurrence of chronic graft deterioration in liver grafts.
- Published
- 2005
10. MAINTENANCE IMMUNOSUPPRESSION WITH CNI AND EVEROLIMUS AFTER ABO INCOMPATIBLE LIVING RELATED KIDNEY TRANSPLANTATION
- Author
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A. Vernauer, Martina Koch, L. Schewior, Lutz Fischer, Bjoern Nashan, Friedrich Thaiss, W. Ternschert, and M. Strecker
- Subjects
Transplantation ,medicine.medical_specialty ,Everolimus ,business.industry ,medicine.medical_treatment ,ABO blood group system ,medicine ,Urology ,Immunosuppression ,medicine.disease ,business ,Kidney transplantation ,medicine.drug - Published
- 2010
11. Make the grade for Wegener's granulomatosis after kidney transplantation.
- Author
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Schewior L, Dragun D, Rudolph B, and Schaeffner E
- Abstract
Antineutrophil cytoplasmic antibodies-associated vasculitis (AAV) is a well-described cause of multiple organ involvement including rapidly progressive pauci-immune crescentic glomerulonephritis. Kidney transplantation (KTx) is considered the treatment of choice in patients with end-stage renal disease (ESRD) due to AAV. Patient and graft survival in AAV after KTx is favourable and comparable with other non-diabetic causes of ESRD. While relapse of AAV is high in dialysis patients (up to 50%), it decreases after KTx (8.6-22.2%). Yet, relapse may occur at any time after KTx and transplant involvement has been documented in at least 25 cases. Therapeutic guidelines for the management of AAV after KTx do not exist and clinical management is a controversial discussion. We present two unusual cases of young males with smouldering AAV who recently underwent KTx at our hospital. Case 1 experienced repeated relapses after KTx and was finally successfully treated with rituximab. Case 2 received rituximab pre-emptively before living kidney donation and remained free of flairs. Prompted by theses two cases, we reviewed the literature focusing on the right point of time for transplantation, risk assessment, role of antineutrophil cytoplasmic antibodies, clinical presentation of flairs and immunosuppression in smouldering Wegener's granulomatosis (WG) and in relapse, including individualized treatment with rituximab.
- Published
- 2009
- Full Text
- View/download PDF
12. The challenge of Wegener's granulomatosis after kidney transplantation.
- Author
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Schewior L, Dragun D, and Schaeffner E
- Subjects
- Antibodies, Antineutrophil Cytoplasmic blood, Granulomatosis with Polyangiitis immunology, Humans, Immunosuppression Therapy, Male, Recurrence, Risk Assessment, Granulomatosis with Polyangiitis therapy, Kidney Transplantation
- Published
- 2009
- Full Text
- View/download PDF
13. The influence of late acute rejection episodes on long-term graft outcome after liver transplantation.
- Author
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Junge G, Tullius SG, Klitzing V, Schewior L, Pratschke J, Radke C, Neuhaus R, and Neuhaus P
- Subjects
- Acute Disease, Follow-Up Studies, Graft Rejection pathology, Humans, Liver Function Tests, Liver Transplantation mortality, Liver Transplantation pathology, Retrospective Studies, Survival Analysis, Time Factors, Treatment Outcome, Graft Rejection physiopathology, Liver Transplantation immunology
- Abstract
Acute cellular rejection represents the most important single risk factor for the occurrence of chronic rejection after organ transplantation. We correlated late acute rejections with the occurrence of chronic graft failure after liver transplantation. We followed 1426 liver transplants for late acute rejection episodes defined as occurring >3 months after OLT. The overall incidence of chronic rejection in our patient population was 3.7%. In summary, we observed a predictive increase of transaminase levels prior to routine biopsies among patients with histologic evidence of late acute rejections. In contrast to other organ systems, late acute rejection episodes were not associated with the occurrence of chronic graft deterioration in liver grafts.
- Published
- 2005
- Full Text
- View/download PDF
14. Withdrawal of steroids: a randomized prospective study of prednisone and tacrolimus versus mycophenolate mofetil and tacrolimus in liver transplant recipients with autoimmune hepatitis.
- Author
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Junge G, Neuhaus R, Schewior L, Klupp J, Guckelberger O, Langrehr JM, Tullius S, and Neuhaus P
- Subjects
- Adult, Anti-Inflammatory Agents adverse effects, Bone Density, Drug Administration Schedule, Drug Therapy, Combination, Female, Follow-Up Studies, Glycated Hemoglobin metabolism, Humans, Immunosuppressive Agents adverse effects, Immunosuppressive Agents therapeutic use, Liver Transplantation immunology, Male, Mycophenolic Acid therapeutic use, Prednisone adverse effects, Time Factors, Anti-Inflammatory Agents therapeutic use, Hepatitis, Autoimmune surgery, Liver Transplantation physiology, Mycophenolic Acid analogs & derivatives, Prednisone therapeutic use, Tacrolimus therapeutic use
- Abstract
The aim of this study was to evaluate the success of steroid (PRED) withdrawal due to replacement by mycophenolate mofetil (MMF) in orthotopic liver transplant (OLT) recipients with autoimmune hepatitis (AIH). Thirty patients with AIH > 12 months after OLT randomized to receive either PRED and tacrolimus (TAC) or MMF and TAC were followed for 24 months. Withdrawal of steroids showed no difference regarding graft and patient survival. Also we demonstrated significantly lower glucose levels with lower HbA1c and a reduced need for insulin as well as a significantly lower serum cholesterol in the MMF group. Patients without steroids showed a lower incidence of osteopenia. Maintenance therapy in OLT patients with AIH may be performed safely using MMF instead of prednisone.
- Published
- 2005
- Full Text
- View/download PDF
15. Acute effects of N-acetylcysteine on skeletal muscle microcirculation following closed soft tissue trauma in rats.
- Author
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Schaser KD, Bail HJ, Schewior L, Stover JF, Melcher I, Haas NP, and Mittlmeier T
- Subjects
- Animals, Cell Communication, Endothelial Cells physiology, Immunohistochemistry, Laser-Doppler Flowmetry, Leukocytes physiology, Male, Microcirculation drug effects, Nitric Oxide physiology, Rats, Rats, Sprague-Dawley, Acetylcysteine pharmacology, Muscle, Skeletal blood supply, Soft Tissue Injuries physiopathology
- Abstract
Trauma-induced microcirculatory dysfunction, formation of free radicals and decreased endothelial release of nitric oxide (NO) contribute to evolving tissue damage following skeletal muscle injury. Administration of N-acetylcysteine (NAC) known to scavenge free radicals and generate NO is considered a valuable therapeutic approach. Thus, the objective of this study was to quantitatively analyze the acute effects of NAC on skeletal muscle microcirculation and leukocyte-endothelial cell interaction following severe standardized closed soft tissue injury (CSTI). Severe CSTI was induced in the hindlimbs of 14 male anesthetized Sprague-Dawley rats using the controlled impact injury technique. Rats were randomly assigned (n = 7) to high-dose intravenous infusion of NAC (400 mg/kg body weight) or isovolemic normal saline (NS). Non-injured, sham-operated animals (n = 7) were subjected to the same surgical procedures but did not receive any additional fluid. Creatin kinase (CK) activity was assessed at baseline, 1 h before and 2 h following posttraumatic NAC or NS infusion. Microcirculation of the extensor digitorum longus (EDL) muscle was analyzed using intravital microscopy and Laser-Doppler flowmetry (LDF). Edema index (EI) was calculated by measuring the EDL wet-to-dry weight ratio (EI=injured/contralateral limb). EDL-muscles were analyzed for desmin immunoreactivity and granulocyte infiltration. Microvascular deteriorations observed following NS-infusion were effectively reversed by NAC: Functional capillary density was restored to levels found in sham-operated animals and leukocyte adherence was significantly (p < 0.05) reduced compared to the NS group. NAC significantly (p < 0.05) increased erythrocyte flux determined by Laser-Doppler flowmetry. Posttraumatic serum CK levels and EI were significantly (p < 0.05) decreased by NAC. During the posttraumatic acute phase, single infusion of NAC markedly reduced posttraumatic microvascular dysfunction, attenuated both leukocyte adherence and tissue infiltration. NAC also decreased CSTI-induced edema formation and myonecrosis as reflected by attenuated serum CK levels and attenuated loss of desmin immunoreactivity. NAC may serve as an effective therapeutic strategy by supporting microvascular blood supply and tissue viability in the early posttraumatic period. Additional studies aimed at long-term analysis and investigation of injury severity--or dosage dependency are needed.
- Published
- 2005
- Full Text
- View/download PDF
16. Massive haemolysis after intramuscular diclofenac in a patient who apparently tolerated oral medication.
- Author
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Ahrens N, Schewior L, Garbe E, Kiesewetter H, and Salama A
- Subjects
- Administration, Oral, Aged, Anemia, Hemolytic complications, Anemia, Hemolytic diagnosis, Anemia, Hemolytic, Autoimmune diagnosis, Antibodies blood, Diagnosis, Differential, Diclofenac administration & dosage, Diclofenac immunology, Female, Humans, Injections, Intramuscular, Renal Insufficiency etiology, Anemia, Hemolytic chemically induced, Diclofenac adverse effects
- Abstract
Background and Objectives: Administration of diclofenac may lead to immune haemolytic anaemia (IHA) owing to the presence of drug-dependent antibodies and/or autoantibodies. A relationship with oral or intramuscular drug administration is unknown. Here, we describe a patient who apparently tolerated oral diclofenac but developed severe IHA following intramuscular injection of the drug., Patients and Methods: A 66-year-old-female was admitted to hospital because of jaundice and nausea, which were initially presumed to be manifestations of a postcholecystectomy syndrome. The patient soon developed haemolysis and renal failure. Although the symptoms and signs were suggestive of autoimmune haemolytic anaemia (AIHA), the patient had diclofenac-induced IHA., Results: Serological testing, including detection of drug-dependent antibodies, was performed using standard techniques. The patient's serum was found to contain a highly reactive diclofenac-dependent red cell antibody of the immune complex type (titre 256 000). She recovered after 7 weeks of treatment with prednisolone, blood transfusions, haemodialysis and plasma exchange., Conclusions: Diclofenac-induced IHA should always be considered when a patient on diclofenac develops haemolysis.
- Published
- 2004
- Full Text
- View/download PDF
17. Small volume hypertonic hydroxyethyl starch reduces acute microvascular dysfunction after closed soft-tissue trauma.
- Author
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Mittlmeier T, Vollmar B, Menger MD, Schewior L, Raschke M, and Schaser KD
- Subjects
- Acute Disease, Animals, Laser-Doppler Flowmetry, Male, Microcirculation, Rats, Rats, Sprague-Dawley, Vascular Diseases etiology, Hydroxyethyl Starch Derivatives therapeutic use, Hypertonic Solutions therapeutic use, Plasma Substitutes therapeutic use, Soft Tissue Injuries complications, Vascular Diseases prevention & control
- Abstract
A major pathway of closed soft-tissue injury is failure of microvascular perfusion combined with a persistently enhanced inflammatory response. We therefore tested the hypothesis that hypertonic hydroxyethyl starch (HS/HES) effectively restores microcirculation and reduces leukocyte adherence after closed soft-tissue injury. We induced closed soft-tissue injury in the hindlimbs of 14 male isoflurane-anaesthetised rats. Seven traumatised animals received 7.5% sodium chloride-6% HS/HES and seven isovolaemic 0.9% saline (NS). Six non-injured animals did not receive any additional fluid and acted as a control group. The microcirculation of the extensor digitorum longus muscle (EDL) was quantitatively analysed two hours after trauma using intravital microscopy and laser Doppler flowmetry, i.e. erythrocyte flux. Oedema was assessed by the wet-to-dry-weight ratio of the EDL. In NS-treated animals closed soft-tissue injury resulted in massive reduction of functional capillary density (FCD) and a marked increase in microvascular permeability and leukocyte-endothelial cell interaction as compared with the control group. By contrast, HS/HES was effective in restoring the FCD to 94% of values found in the control group. In addition, leukocyte rolling decreased almost to control levels and leukocyte adherence was found to be reduced by approximately 50%. Erythrocyte flux in NS-treated animals decreased to 90 +/- 8% (mean SEM), whereas values in the HS/HES group significantly increased to 137 +/- 3% compared with the baseline flux. Oedema in the HS/HES group (1.06 +/- 0.02) was significantly decreased compared with the NS-group (1.12 +/- 0.01). HS/HES effectively restores nutritive perfusion, decreases leukocyte adherence, improves endothelial integrity and attenuates oedema, thereby restricting tissue damage evolving secondary to closed soft-tissue injury. It appears to be an effective intervention, supporting nutritional blood flow by reducing trauma-induced microvascular dysfunction.
- Published
- 2003
- Full Text
- View/download PDF
18. In vivo analysis of microcirculation following closed soft-tissue injury.
- Author
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Schaser KD, Vollmar B, Menger MD, Schewior L, Kroppenstedt SN, Raschke M, Lübbe AS, Haas NP, and Mittlmeier T
- Subjects
- Animals, Blood Pressure, Capillary Permeability physiology, Cell Adhesion immunology, Cell Communication immunology, Edema physiopathology, Endothelium, Vascular cytology, Endothelium, Vascular immunology, Heart Rate, Leukocytes cytology, Male, Microcirculation physiology, Pressure, Rats, Disease Models, Animal, Muscle, Skeletal blood supply, Muscle, Skeletal injuries, Rats, Sprague-Dawley, Soft Tissue Injuries physiopathology
- Abstract
Major loss of tissue is an almost invariable consequence of severe closed soft-tissue injury. Clinically, the extent of soft-tissue trauma determines the outcome of complex injuries and significantly influences bone healing. With use of a new animal model, this study quantitatively analyzed microcirculation, i.e., nutritive perfusion and leukocyte-endothelial cell interaction, in skeletal muscle after standardized closed soft-tissue injury. By means of a computer-assisted controlled-impact technique, a severe standardized closed soft-tissue injury was induced in the left hindlimb of 28 rats. The rats were assigned to four experimental groups (n = 7 per group) that differed by time of analysis (1.5, 24, 72, and 120 hours after injury); rats that were not injured served as controls (n = 7). Intramuscular pressure was measured, and microcirculation in the rat extensor digitorum longus muscle was analyzed by in vivo fluorescence microscopy, which allowed assessment of microvascular diameters, functional capillary density, number of rolling and adherent leukocytes in venules, and microvascular permeability. Edema weight gain was quantified by the ratio of wet to dry weight of the extensor digitorum longus muscle. Microvascular perfusion of the skeletal muscle was characterized by a significant reduction in functional capillary density, which was paralleled by an increase in capillary diameter throughout the 120 hours of observation when compared with the controls. Trauma-induced inflammatory response was reflected by a markedly increased rolling and adherence of leukocytes, primarily restricted to the endothelium of postcapillary venules; this was accompanied by increased microvascular permeability, indicative of a substantial loss of endothelial integrity. The microcirculation surrounding the core of the damaged tissue area resembled that of ischemia-reperfusion injury in skeletal muscle, i.e., heterogeneous capillary perfusion, pronounced microvascular leakage, and adherence of leukocytes. Enhanced vascular leakage and leukocyte adherence (24-72 hours after injury) coincided with the maximum intramuscular pressure (which was not indicative of compartment syndrome) and edema formation. These results demonstrate that initial changes, leading to ultimate tissue death, after closed soft-tissue injury are caused on the microcirculatory level. This standardized model provides further insight into microvascular pathophysiology and cellular interactions following closed soft-tissue injury. Thus, it is an adequate tool for testing novel therapeutic interventions.
- Published
- 1999
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